Superior canal dehiscence reveals concomitant unilateral utricular loss (UUL)

Conclusion: We report enhanced symmetrical cervical vestibular evoked myogenic potential (cVEMP) but asymmetrical ocular VEMP (oVEMP) responses in a patient with CT-verified bilateral superior semicircular canal dehiscence (SCD) but with acute vestibular syndrome. This implies that absence of unilateral utricular macula function alone is sufficient to cause symptoms of acute vertigo. Acute vertigo should not automatically be presumed to originate from semicircular canal dysfunction. Objectives: To identify the cause of an acute vertigo attack in a patient with bilateral SCD. Methods: The functional state of all peripheral vestibular sense organs was tested using the video head impulse test (vHIT) for all semicircular canals and VEMPs to air-conducted sound (ACS) or bone-conducted vibration (BCV) to test all otolith organs. The cVEMP tested mainly saccular function and the oVEMP mainly utricular function. Results: All semicircular canals showed normal function. The cVEMPs showed enhanced, but symmetrical saccular function. In contrast, oVEMPs showed an enhanced but asymmetric n10 component – it was greatly reduced beneath the left eye, implying decreased function in the right utricular macula. That result was confirmed using very high frequency stimuli which are effective in SCD: 4000 Hz BCV stimuli showed that oVEMP n10 was present beneath the right eye but absent beneath the left eye.     

Head-Shaking Nystagmus Depends on Gravity

In acute unilateral peripheral vestibular deficit, horizontal spontaneous nystagmus (SN) increases when patients lie on their affected ear. This phenomenon indicates an ipsilesional reduction of otolith function that normally suppresses asymmetric semicircular canal signals. We asked whether head-shaking nystagmus (HSN) in patients with chronic unilateral vestibular deficit following vestibular neuritis is influenced by gravity in the same way as SN in acute patients. Using a three-dimensional (3-D) turntable, patients (N = 7) were placed in different whole-body positions along the roll plane and oscillated (1 Hz, ±10°) about their head-fixed vertical axis. Eye movements were recorded with 3-D magnetic search coils. HSN was modulated by gravity: When patients lay on their affected ear, slow-phase eye velocity significantly increased upon head shaking and consisted of a horizontal drift toward the affected ear (average: 1.2°/s ±0.5 SD), which was added to the gravity-independent and directionally nonspecific SN. In conclusion, HSN in patients with chronic unilateral peripheral vestibular deficit is best elicited when they are lying on their affected ear. This suggests a gravity-dependent mechanism similar to the one observed for SN in acute patients, i.e., an asymmetric suppression of vestibular nystagmus by the unilaterally impaired otolith organs.     

Horizontal vestibulo-ocular reflex dynamics in acute vestibular neuritis and viral labyrinthitis: evidence of otolith-canal interaction

Objective To evaluate the dynamic properties of the horizontal vestibulo-ocular reflex (h-VOR) in the acute stage of two common labyrinthine diseases that provoke severe attacks of vertigo with spontaneous nystagmus: vestibular neuritis (vestibular loss alone) and viral labyrinthitis (cochleovestibular loss).

Material and Methods Sixty-three patients were investigated: 42 were diagnosed with vestibular neuritis and 21 with viral labyrinthitis. The h-VOR function was evaluated by conventional caloric and impulsive testing. A simplified model of vestibular function was used to analyze the vestibulo-ocular response to rotational stimulation.

Results The results showed a significant difference in h-VOR characteristics between the two pathologies. Patients with vestibular neuritis exhibited a strong horizontal semicircular canal deficit, but no h-VOR asymmetry between the two rotational directions. In contrast, patients with viral labyrinthitis demonstrated moderate canal paresis and a marked h-VOR deficit in rotation toward the affected ear.

Conclusions These findings support the hypothesis that the h-VOR dynamic asymmetry that occurs after an acute unilateral inner ear lesion is not due to canal dysfunction alone, but involves complex adaptive changes in the central VOR that may implicate the otolith system. Based on histopathologic and clinical differences in the two pathologies reported in the literature, we postulate that this otolith-canal interaction is mainly linked to the loss of saccular function.     

A new method to improve the imbalance in chronic unilateral vestibular loss: the organization of refixation saccades

Conclusion: VOR adaptation and organization of refixation saccades in a gathered pattern is a process that can be artificially induced in patients with unilateral vestibular loss who have not developed it naturally, improving imbalance and vestibular disability.

Objective: To test that temporary grouping of refixation saccades should be linked to better clinical status without gain recovery.

Methods: A training to induce the refixation saccades into gathered fashion is performed. The outcome measures are handicap level measured by the dizziness handicap index (DHI) and refixation saccades organization pattern measured by a numeric score called ‘PR’ given by a software developed by the authors. Analysis is done before the training and 1 and 3 months after ending, Non-parametric tests were used for statistical analysis.

Results: This study has included 10 healthy subjects (four males, six females), and 16 patients with chronic unsteadiness due to unilateral vestibular loss (nine vestibular neuritis, four post-surgical vestibular schwannoma, and three cases after intra-tympanic gentamycin in patients with Ménière’s disease). The reduction in the DHI score was significant at 1 (p?=?0.028) and 3 months (p?=?0.042) post-treatment. Also, statistically significant differences were found between the PR score before and PR score 1 (p?=?0.005) and 3 months after the treatment (p?=?0.003).     

Functional loss of the horizontal doll's eye reflex following unilateral vestibular lesions

The doll's eye reflex represents the vestibulo-ocular reflex (VOR) elicited by high-acceleration head rotation. After complete unilateral vestibular lesions, the ipsilateral, horizontal doll's eye reflex is replaced by a series of “catch-up” saccades. These cause permanent symptoms of blurred vision and dizziness during ipsilateral turns. We compared normal controls and patients with complete surgical lesions or canal paresis of up to 9 years duration via electronystagmography (ENG) to determine the usefulness of the doll's eye test as a diagnostic test for complete vestibular lesions. This test was found to be more sensitive in diagnosis of such lesions than head-shaking nystagmus, rotatory directional preponderance, and spontaneous nystagmus. It is also useful to document VOR function in patients in whom caloric irrigation is contraindicated.     

Caloric and Search-Coil Head-Impulse Testing in Patients after Vestibular Neuritis

The objective of this study was to compare results of quantitative head-impulse testing using search coils with eye-movement responses to caloric irrigation in patients with unilateral vestibular hypofunction after vestibular neuritis. The study population consisted of an acute group (<3 days; N = 10; 5 male, 5 female; 26-89 years old) and a chronic group (>2 months; N = 14; 8 male, 6 female; 26-78 years old) of patients with unilateral vestibular hypofunction after vestibular neuritis. The testing battery included: (1) simultaneous measurement of eye and head rotations with search coils in a magnetic coil frame during passive Halmagyi-Curthoys head-impulse testing and (2) electronystagmography during bilateral monaural 44 degrees C-warm and 30 degrees C-cold caloric irrigation. The main outcome measures were (1) the gain of the horizontal vestibulo-ocular reflex during search-coil head-impulse testing and (2) the amount of canal paresis during caloric irrigation. All acute and chronic patients had a unilateral gain reduction during search-coil head-impulse testing. A pathological canal paresis factor was present in 100% of the acute patients but in only 64% of the chronic patients. The clinically suspected unilateral vestibular hypofunction resulting from vestibular neuritis was validated in all acute patients by both search-coil head-impulse and caloric testing. Hence, either of these tests is sufficient for diagnosis in the acute phase of vestibular neuritis. Chronic patients, however, were reliably identified only by search-coil head-impulse testing, which suggests that the low-frequency function of the labyrinths often becomes symmetrical, leading to a normal canal paresis factor.     

Detection of isolated covert saccades with the video head impulse test in peripheral vestibular disorders

Objectives

The function of the semicircular canal receptors and the pathway of the vestibulo-ocular-reflex (VOR) can be diagnosed with the clinical head impulse test (cHIT). Recently, the video head impulse test (vHIT) has been introduced but so far there is little clinical experience with the vHIT in patients with peripheral vestibular disorders. The aim of the study was to investigate the horizontal VOR (hVOR) by means of vHIT in peripheral vestibular disorders.

Methods

Using the vHIT, we examined the hVOR in a group of 117 patients and a control group of 20 healthy subjects. The group of patients included vestibular neuritis (VN) (n = 52), vestibular schwannoma (VS) (n = 31), Ménière's disease (MD) (n = 22) and bilateral vestibulopathy (BV) (n = 12).

Results

Normal hVOR gain was at 0.96 ± 0.08, while abnormal hVOR gain was at 0.44 ± 0.20 (79.1% of all cases). An abnormal vHIT was found in VN (94.2%), VS (61.3%), MD (54.5%) and BV (91.7%). Three conditions of refixation saccades occurred frequently in cases with abnormal hVOR: isolated covert saccades (13.7%), isolated overt saccades (34.3%) and the combination of overt and covert saccades (52.0%).

Conclusions

The vHIT detects abnormal hVOR changes in the combination of gain assessment and refixation saccades. Since isolated covert saccades in hVOR changes can only be seen with vHIT, peripheral vestibular disorders are likely to be diagnosed incorrectly with the cHIT to a certain amount.     

Diagnostic value of eye movement and vestibular function tests in patients with posterior circulation infarction

Objective: To evaluate the diagnostic value of eye movements and vestibular function tests in PCI patients.

Methods: Thirty-eight PCI patients and 31 patients with unilateral vestibular neuritis (UVN) were enrolled and underwent eye movement tests and vestibular function tests (spontaneous nystagmus [SN], head-shaking nystagmus [HSN]).

Results: The rates of eye movement abnormality were 78.9% and 41.9% in PCI and UVN patients, respectively. The positive rate of SN and HSN were, respectively, 41.2% and 43.8% in cerebellar infarction patients, 33.3% and 66.7% in medullary infarction patients, and 100.0% and 86.2% in UVN patients. The horizontal direction of SN and HSN coincided with the affected side in cerebellar infarction patients, and the healthy side in UVN patients, which coincided with the healthy side and the affected side, respectively in medullary infarction patients. The horizontal direction of HSN was bidirectional nystagmus in 16.0% (4/25) of UVN patients.

Conclusions and significance: Eye movement and vestibular function tests contribute to the early diagnosis of PCI. The horizontal direction of SN and HSN are consistently toward the affected side in cerebellar infarction patients and the healthy side in UVN patients, in contrast to medullary infarction patients, and deserve further investigations.     

Dynamics of canal response to head-shaking test in benign paroxysmal positional vertigo

Conclusions. Time constant and maximum slow phase velocity (SPV) of head-shaking nystagmus (HSN) demonstrated a differential canal response to head shaking in 24% of patients with posterior canal benign paroxysmal positional vertigo (BPPV). We suggest that vestibular lithiasis has a limited contribution to the mechanism that generates HSN. Objective. To determine the canal response to head shaking in BPPV. Patients and methods. This was a case-control study including 104 individuals with BPPV. The diagnosis was based on the presence of vertigo and nystagmus during the positional test. Subjects were examined by the horizontal and vertical head-shaking test. Eye movements were recorded on a video camera to analyze the nystagmus. The head was shaken passively in the horizontal and sagittal planes, respectively, for horizontal and vertical HSN at a frequency of 2 Hz. HSN was considered when six consecutive beats of nystagmus with an SPV of at least 2°/s were detected. Main outcome measures were the presence of horizontal and vertical HSN, maximum SPV of HSN, time constant of HSN, and canal paresis. Results. Maximum SPV of vertical HSN was higher in BPPV patients with posterior canal BPPV (n=10) than in controls (p=0.04). Moreover, the time constant of vertical HSN was significantly lower for posterior canal BPPV when compared with controls (p<0.02).     

3D analysis of spontaneous nystagmus in early stage of vestibular neuritis

Objective

The pathological localization of vestibular neuritis is still controversial. Analyses of the spontaneous nystagmus support the temporal bone studies, which indicated the location of the pathology to be in the superior vestibular nerve. However, based on the data from the head impulse testing the pathology is in the vestibular nerve including the inferior branch.

Methods

Twenty-three patients with vestibular neuritis participated in this study. The spontaneous nystagmus was recorded within 1 week after the onset of the disease. Three-dimensional analysis of the nystagmus was performed using video image analysis system. The rotation axis was calculated and compared to the anatomical axes of the semicircular canals.

Results

The axes of the spontaneous nystagmus in all patients were scattered around the axes of horizontal and anterior canals, especially between the compound axis of anterior and horizontal canals and the axis of horizontal canal. The statistical analysis revealed that in the quite early stage of the disease (day 0–2 of the attack), the spontaneous nystagmus tended to have more torsional eye movements as compared to the less early stage (day 3–6).

Conclusion

The present study strongly suggests that the pathology of vestibular neuritis is in the superior vestibular nerve branch. Also it can be speculated that at the early stage of this disease, the pathology is in the whole branch of the nerve. Subsequently, the anterior canal branch recovers faster than the horizontal canal branch.     

Der Video-Kopfimpulstest

Background

Side-specific test procedures are mandatory in order to assess the function of peripheral vestibular receptors. Semicircular canals (SCC) and vestibulo-ocular reflex (VOR) can be tested by the Halmagyi and Curthoy head impulse test (HIT) and recently by means of the video head impulse test (vHIT). The vHIT procedure is a new method to measure eye and head velocity during brief and rapid head impulses. This method provides objective information of VOR and detects both overt and covert catch-up saccades.

Materials and methods

As clinical experiences with vHIT are limited, in this study the horizontal VOR (hVOR) was examined by means of the vHIT in 142 consecutive patients with acute or chronic vestibular syndrome.

Results

A total of 20 healthy volunteers served as a control group and exhibited a normal average VOR gain of 0.97?±?0.09 without re-fixation saccades. In patients, 47.6% showed a pathological vHIT whereas 52.4% revealed a normal test result. Covert catch-up saccades could be revealed in 13.7% by means of vHIT whereas in 86.3% overt catch-up saccades alone or in combination with covert catch-up saccades were found in the majority of catch-up saccades in peripheral vestibular disorders.

Conclusions

By means of the vHIT it is possible to obtain a side-specific and quantitative assessment of hVOR. Video-head impulse test is a reliable tool for vestibular testing even in bedside examinations of patients suffering from dizziness.     

Recovery of vestibular evoked myogenic potentials after a vertigo attack due to vestibular neuritis

Conclusions. Inferior vestibular nerve functions could recover in patients with vestibular neuritis (VN).

Objectives. Although the recovery of superior vestibular nerve functions has been reported, there is little information about the recovery of inferior vestibular nerve functions in patients with VN. This study was done to clarify if inferior vestibular nerve functions recover after an attack of VN.

Methods. Neuro-otological tests including vestibular evoked myogenic potential (VEMP) testing and caloric testing were sequentially performed in 13 patients with VN, who showed absence of VEMP on the affected side at the initial examination (7 men and 6 women, 28–82 years of age). VEMPs to click stimulation (95 dBnHL) were recorded with surface electrodes over each sternocleidomastoid muscle.

Results. Among the 13 patients, 5 patients (4 men and 1 woman) showed recovery of VEMP responses. Four of the five patients (three men and one woman) showed recovery of VEMP to the normal range. It takes 6 months to 2 years to recover within the normal range. On the other hand, caloric responses recovered to the normal range only in one patient.     

Evidence of vestibular and balance dysfunction in children with profound sensorineural hearing loss using cochlear implants

Objectives/Hypothesis: Similarities between the peripheral auditory and vestibular systems suggest that children with sensorineural hearing loss (SNHL) may demonstrate vestibular and balance impairments. This hypothesis was studied in 40 children with severe to profound SNHL and unilateral cochlear implants. Study Design: Prospective cross‐sectional study with repeated measures. Methods: Vestibular function was assessed with caloric, rotational, and vestibular evoked myogenic potential testing; balance was assessed using the balance subset of the Bruininks‐Oseretsky Test of Motor Proficiency‐II, a standardized test of static and dynamic balance. Results: Horizontal semicircular canal function was abnormal in response to a caloric stimulus in 50% (16/32), with a large proportion of those [6/16 (38%)] reflecting mild to moderate unilateral abnormalities. In comparison, horizontal semicircular canal function in response to rotation was abnormal in 38% (14/37). Saccular function was absent bilaterally in 5/26 (19%) and unilaterally in 5/26 (19%) with vestibular evoked myogenic potential. Age standardized balance abilities were significantly poorer in the study population [μ = 12.9 ± 5(SD)] compared with normal hearing controls [μ = 17 ± 5(SD); P = .0006] and correlated best with horizontal canal function in response to a rotational stimulus (P = .004; R² = 0.24). SNHL from meningitis was associated with worse balance function than other etiologies. Conclusions: Vestibular and balance dysfunction occurred in >1/3 of children with SNHL and cochlear implants, and is highly dependent on etiology. Although compliance with all tests was high, rotational chair testing, which assesses higher frequency motion (0.25–5 Hz) and thus more “real world” vestibular function, correlated best with dynamic balance. For this reason, rotational chair testing may represent the test of choice in this population, particularly given that it is amenable to testing children of all ages.     

Acute vestibular asymmetry disorder: a new disease entity in acute vestibular syndrome?

Background: Acute vestibular syndrome (AVS) is characterized by the rapid onset of vertigo, nausea, vomiting and gait unsteadiness, which lasts for days.

Aims/objectives: We report cases as acute vestibular asymmetry disorder (AVAD), with presentations that mimic vestibular neuritis (VN) but without central lesions.

Materials and methods: We retrospectively reviewed records of patients presenting with acute spontaneous vertigo lasting more than 24?h from January 2011 to June 2016. Among 341 patients, five showed different findings that did not indicate either VN or stroke. We analyzed the clinical features and vestibular assessments of these patients.

Results: All five patients showed spontaneous nystagmus continuing for several days. However, head impulse tests (HITs) did not reveal a corrective saccade. Brain magnetic resonance imaging showed no abnormal lesions. The bithermal caloric test revealed directional preponderance without canal paresis. Finally, the slow harmonic test of the rotatory chair revealed unilateral high gain and phase within the normal range, but a significantly asymmetric response was observed. No patients showed recurrence during follow-up.

Conclusions and significance: Our study suggests that a normal HIT in AVS is not always a dangerous sign indicating an acute stroke. From our observations, we propose that AVAD would be a new disease entity within AVS.     

Head impulses after unilateral vestibular deafferentation validate Ewald's second law.

To determine the relative contributions of ampullofugal (AF) and ampullopetal (AP) stimulation of the horizontal semicircular canal (HSCC) to the horizontal vestibulo-ocular reflex (HVOR), 12 patients were studied 1 year after total unilateral vestibular deafferentation (UVD). Compensatory eye movement responses to impulses of horizontal head rotation were studied using magnetic search coils. The head impulses were rapid (up to 3000 deg/sec/sec) passive, unpredictable, step displacements of horizontal angular head position with respect to the trunk. The results from these 12 patients were compared with results from 30 normal subjects. An HVOR deficit was found to each side. The HVOR in response to head impulses toward the deafferented side, a response generated exclusively by ampullofugal stimulation of the single functioning HSCC, was severely deficient with an average gain of 0.25; the HVOR in response to head impulses toward the intact side, a response generated exclusively by ampullopetal stimulation of the single functioning HSCC, was mildly but significantly deficient compared with normal subjects. These results show that rapid, unpredictable head movements, unlike slow, predictable head movements, do demonstrate the AP-AF HVOR asymmetry, which could be expected from consideration of the behavior of single vestibular afferent neurons, an asymmetry that is expressed by Ewald's 2nd Law.     

MRI of the vestibular nerve after selective vestibular neurectomy

Conclusion. In patients with Ménière's disease and persisting vertigo attacks after vestibular neurectomy (VNx) MRI of the vestibulocochlear nerve can identify residual vestibular nerve fibres that could be responsible for the vertigo attacks. Objective. To test if MRI of the vestibulocochlear nerve can corroborate the presence of residual vestibular nerve fibres in patients with persisting vertigo attacks and residual vestibular function after VNx. Materials and methods. Vestibulocochlear nerve bundles of seven post-VNx unilateral Ménière's patients were imaged using 1.5 Tesla MRI with steady state free precession (SSFP) sequences. Reformatted MR images orthogonal to the vestibulocochlear nerve axis in internal auditory canal were compared on the VNx and intact sides. Vestibular function was assessed with caloric tests, three-dimensional head impulse tests and vestibular evoked myogenic potentials. Of the seven patients only one was asymptomatic (totally free of vertigo); six had continued to experience vertigo attacks, albeit not as long or as severe as before VNx. Results. On the VNx side, MRI showed intact facial and cochlear nerves in all seven patients. In the six symptomatic patients, although superior and inferior vestibular nerve bulk and signal were reduced, residual bulk suggestive of inferior vestibular nerve was evident, correlating with evidence of residual posterior canal function on impulsive testing in all six symptomatic patients. In the asymptomatic patient, superior and inferior vestibular nerves were absent on MRI and impulsive testing revealed no residual posterior canal function.     

Symptomatic high frequency/acceleration vestibular loss: consideration of a new clinical syndrome of vestibular dysfunction

Conclusion Symptomatic high frequency/acceleration vestibular loss is a distinct clinical entity that can be missed on conventional ENG with caloric testing. Under certain circumstances, symptomatic patients with a high frequency/acceleration vestibular loss should undergo an MSSC study for confirmation, if required.

Objective To document that normal electronystagmography (ENG) with conventional bithermal caloric testing is inadequate for diagnosing clinically significant high frequency/acceleration vestibular loss.

Material and methods Patients with clinical symptoms and signs of persistent peripheral vestibular dysfunction despite normal conventional bithermal caloric testing on ENG underwent high frequency/acceleration horizontal magnetic scleral search coil (MSSC) eye movement studies. The clinical findings and results from audiometric tests, conventional ENG with bithermal caloric tests and MSSC tests were reviewed.

Results Eleven patients were identified as having an abnormal MSSC study, indicating a high frequency/acceleration vestibular loss consistent with their clinical history despite normal or equivocal bithermal caloric responses on conventional ENG. Although valuable, ENG caloric testing evaluates lateral semicircular canal function and should be considered a non-physiological test primarily of low frequency vestibular function. High frequency/acceleration head thrust testing clinically detected a “high frequency/acceleration vestibular loss” in 8/11(72.7%) cases.     

Unilateral Adaptation of the Human Angular Vestibulo-Ocular Reflex

A recent study showed that the angular vestibulo-ocular reflex (VOR) can be better adaptively increased using an incremental retinal image velocity error signal compared with a conventional constant large velocity-gain demand (×2). This finding has important implications for vestibular rehabilitation that seeks to improve the VOR response after injury. However, a large portion of vestibular patients have unilateral vestibular hypofunction, and training that raises their VOR response during rotations to both the ipsilesional and contralesional side is not usually ideal. We sought to determine if the vestibular response to one side could selectively be increased without affecting the contralateral response. We tested nine subjects with normal vestibular function. Using the scleral search coil and head impulse techniques, we measured the active and passive VOR gain (eye velocity / head velocity) before and after unilateral incremental VOR adaptation training, consisting of self-generated (active) head impulses, which lasted ∼15 min. The head impulses consisted of rapid, horizontal head rotations with peak-amplitude 15 ^o, peak-velocity 150 ^o/s and peak-acceleration 3,000 ^o/s². The VOR gain towards the adapting side increased after training from 0.92 ± 0.18 to 1.11 ± 0.22 (+22.7 ± 20.2 %) during active head impulses and from 0.91 ± 0.15 to 1.01 ± 0.17 (+11.3 ± 7.5 %) during passive head impulses. During active impulses, the VOR gain towards the non-adapting side also increased by ∼8 %, though this increase was ∼70 % less than to the adapting side. A similar increase did not occur during passive impulses. This study shows that unilateral vestibular adaptation is possible in humans with a normal VOR; unilateral incremental VOR adaptation may have a role in vestibular rehabilitation. The increase in passive VOR gain after active head impulse adaptation suggests that the training effect is robust.     

Search-coil head-thrust and caloric tests in Ménière's disease

Conclusions. Our findings suggest that canal function is substantially preserved in subjects with active vertigo attacks as a result of Ménière's disease (MD). In these subjects, the head-thrust test (HTT) may not be as sensitive to canal dysfunction as traditional caloric testing. MD may differentially affect the low-frequency sensitivity of the canals. Objective. Caloric tests have traditionally been used to characterize semicircular canal function in vestibular disorders, including MD. The quantitative HTT provides an objective measurement of semicircular canal function in the frequency and velocity ranges of normal head movements. The aim of this study was to compare the findings of caloric and HTTs in subjects with unilateral MD. Material and methods. The study population consisted of 38 candidates for gentamicin treatment due to a high frequency of vertiginous attacks (25 males, 13 females; mean age 52.9 years; range 30–70 years). The duration of symptoms was 1–30 years (mean 5.3 years). Horizontal canal function was characterized with bithermal aqueous caloric tests and recordings of the angular vestibulo-ocular reflexes (aVORs) using the scleral search-coil technique during HTTs. The main outcomes were unilateral weakness (UW) on caloric testing and aVOR gain asymmetry (GA) during HTTs. A caloric response asymmetry of >20% was considered to be indicative of pathologic UW. A difference in GA during HTTs of >5.8% was considered significant. Results. Twenty subjects (52.6%) showed abnormal results on one or both tests. Pathologic UW was present in 16 subjects (42.1%). During HTTs, 11 subjects (28.9%) showed pathologic GA. Seven subjects (18.4%) showed abnormal results on both tests. A significant correlation was found between UW and GA. However, pathologic GA during HTTs in subjects with unilateral MD was less frequent and the values smaller than those published for vestibular neuritis patients. Two subjects with unilateral MD had 100% UW, but none had >30% asymmetry on HTTs.     

Long-term deficits of goal-directed vestibulo-ocular function following total unilateral loss of peripheral vestibular function

Brief whole-body movements (+/- 5 to 170 degrees/s peak velocity; approximately equal to 0.5 s duration), applied during 1.44-s intervals of total darkness while subjects "looked" at a just-viewed target, were used to examine vestibulo-ocular function in 3 patients who had compensated to total unilateral loss of peripheral vestibular function. We found that the combined effects of slow-phase and saccadic eye movements both tended to keep the eyes stabilized on the unseen target. Compensatory slow-phases elicited during rapid head movements ipsilateral to (i.e., towards) the lesion were only about 60% as effective as those elicited during rapid contralateral movements. Compensatory gaze-correcting saccades tended to supplement deficient slow-phase movements, especially during rapid ipsilateral head movement. However, the gaze-correcting effect of saccades was only about half of the required for perfect stabilization. Thus, two functional vestibular deficits were observed during rapid ipsilateral head movements: (1) reduced slow-phase stabilization, and (2) reduced saccadic ability to adequately supplement the deficient slow phases. However, overall vestibular functional capability, as assessed by observation of the net effect of both slow phases and saccades, was much better than would be indicated by conventional observation of slow-phase movements alone.